For a thorough background description of the physiology of a human heart, as well as a description of the basic operation of an implantable pacemaker, reference should be made to the various patents and patent applications cited herein. That which is presented below is a brief summary of such background information.
As is known in the art, the basic function of the heart is to pump (circulate) blood throughout the body thereby delivering oxygen and nutrients to the various tissues and removing waste products and carbon dioxide therefrom. The heart is divided into four chambers comprised of two atria and two ventricles. The atria are the collecting chambers holding the blood that returns to the heart until the ventricles are ready to receive this blood. The ventricles are the primary pumping chambers. The pumping function of the heart is achieved by a coordinated contraction of the muscular walls of the atria and the ventricles.
As is also known in the art, the atria are more than simple collecting chambers. The atria contain the heart's own spontaneous pacemaker, the sinus node, that controls the rate at which the heartbeats or contracts. Furthermore, atrial contraction helps to fill the ventricles, contributing to optimal filling of the ventricles, thus maximizing the amount of blood that the heart is able to pump with each contraction, i.e., maximizing the hemodynamic efficiency of the heart. In the normal heart, an atrial contraction is followed, after a short period of time (normally 120 to 200 ms), by a ventricular contraction, i.e., a conducted R-wave.
The period of cardiac contraction during which the heart actively ejects the blood into the arterial blood vessels is called systole. The period of cardiac relaxation during which the chambers are being filled with blood is called diastole. Atrial and ventricular systole are sequenced allowing the atrial contraction to help optimally fill the ventricle. This sequencing is termed AV synchrony.
A cardiac cycle (or heartbeat) comprises one sequence of systole and diastole. It can be detected by a physician counting the patient's pulse rate. It is also reflected by the cardiac rhythm as recorded on an electrocardiogram. The electrocardiogram (ECG) records the electrical activity of the heart as seen on the surface of the body. The electrical activity corresponds to the electrical cardiac depolarization in either the atrium and/or ventricle. On the ECG, the atrial depolarization is represented by a waveform referred to as the P-wave, while the ventricular depolarization is represented by a waveform referred to as the QRS complex, sometimes abbreviated as an "R-wave."
A normal heart rate varies between 60 to 100 heartbeats (or cardiac cycles) per minute with an average of 72 bpm resulting in approximately 100,000 cardiac cycles per day. The heart rate normally increases during periods of stress (physical or emotional) and slows during periods of rest (sleep).
The amount of blood that the heart pumps in one minute is called the cardiac output. It is calculated by the amount of blood ejected with each heartbeat (stroke volume) multiplied by the number of heartbeats in a minute. If the heart rate is too slow to meet the physiological requirements of the body, the cardiac output will not be sufficient to meet the metabolic demands of the body. One of two major symptoms may result. If the heart effectively stops with no heartbeat, there will be no blood flow and if this is sustained for a critical period of time (10 to 30 seconds), the individual will faint. If there is a heartbeat but it is too slow, the patient will be tired and weak (termed low cardiac output).
Too slow a heartbeat is termed a bradycardia. Any heart rate below a rate of 60 bpm is considered a bradycardia, however bradycardia only needs to be treated if it is a persistent abnormality and causes a patient to have symptoms. In such cases, implantation of a permanent electronic pacemaker is often prescribed.
An electronic pacemaker may also be referred to as a pacing system, or a cardiac pacemaker. The pacing system is comprised of two major components. One component is a pulse generator that includes electronic circuitry and a power cell or battery. The other is a lead or leads which connect the pulse generator to the heart.
Electronic pacemakers are described as either single-chamber or dual-chamber systems. A single-chamber system stimulates and senses the same chamber of the heart (atrium or ventricle). A dual-chamber system stimulates and/or senses in both chambers of the heart (atrium and ventricle). The electronic pacemaker delivers an electrical stimulus to stimulate the heart to contract when the patient's own spontaneous pacemaker (i.e., the sinus node) fails or when conduction of an R-wave is blocked. In this way, the electronic pacemaker can help to stabilize the heart rate of a patient's heart.
Conduction of an R-wave can be blocked in a variety of ways. For example, the atrio-ventricular (AV) node may be partially or completely insensitive to the propagation of a P-wave. Alternately, the Bundle of His or a bundle branch may suddenly stop propagation of the R-wave to the ventricular tissue. Hereinafter, a P-wave which originates in the sinus node shall be referred to as a "spontaneous P-wave," a naturally occurring R-wave which is triggered by either a spontaneous or paced P-wave shall be referred to as a "conducted R-wave," and the AV node, the Bundle of His, etc. shall be referred to as the heart's "conduction system."
Most pacemakers are referred to as demand-type pacemakers. This means that they are capable of sensing the electrical signal in or on the cardiac chamber by way of the pacing lead, which is placed in or on the chamber. The electrical signal as recorded in or on the heart is called an electrogram (EGM), or sometimes an intracardiac electrogram (IEGM), and is a relatively large signal with very rapid changes in electrical potential. The most rapid portion of this signal is called the intrinsic deflection (ID), which is what is sensed by the pacemaker. Although medical personnel commonly talk about pacemakers sensing P-waves or R-waves, this is not technically correct. The P-wave and R-wave, technically, are recorded from the surface of the body. The pacemaker, in contrast, senses the atrial or ventricular intrinsic deflection (ID) portion of the atrial or ventricular electrogram from within the heart. The atrial EGM coincides with the P-wave of the surface ECG while the ventricular EGM coincides with the R-wave of the surface ECG. Thus, the terms P-wave and R-wave are commonly used, and will be used herein, synonymously with the atrial and ventricular intrinsic deflection portions of the atrial and ventricular electrograms.
One of the parameters of the pacemaker that can commonly be programmed or set by the physician is a base rate, which is the lowest heart rate that can be detected in a patient before the pacemaker will begin pacing. If the patient's ventricular heart rate is faster than this base rate, the pacemaker will recognize the ventricular electrical depolarization and be either inhibited or triggered depending upon how the electronic pacemaker is configured (and will reset its various timing cycles) . If the patient's ventricular heart rate slows below the base rate of the electronic pacemaker, the electronic pacemaker's timers will expire (or "time out") and will cause the electronic pacemaker to periodically release an output pulse (electrical stimulation) at the base rate, thus preventing the patient's ventricular heart rate from falling below the base rate.
The interval between consecutive output pulses within the same chamber is termed the automatic interval or basic pacing interval. The interval between a sensed event and the ensuing paced event is called an escape interval. In single-chamber pacing systems, the automatic and escape intervals are commonly identical. In dual-chamber pacing systems, the basic pacing interval is divided into two subintervals. The interval from a sensed R-wave or ventricular paced event to the atrial paced event is called an atrial escape interval. The interval from the sensed P-wave or atrial paced event to the ventricular paced event is called the AV interval (AVI), or AV delay.
In the majority of individuals, the most effective heartbeat is triggered by the patient's own spontaneous pacemaker. The electronic pacemaker is intended to fill in when the patient's spontaneous pacemaker fails or when the heart's conduction system fails. The first pacing mode that was developed was single-chamber ventricular stimulation. It was soon recognized that this resulted in the loss of appropriate synchronization between the atria and ventricles in which case, the hemodynamic efficiency of the heart was compromised and the cardiac output fell despite maintaining an adequate rate. In those patient's whose need for a pacemaker was intermittent, with a normal rhythm occurring between times when pacing support was required, electronic pacemakers were developed which were set to a slow base rate. This allowed the patient's underlying rhythm to slow to this very low base rate before the electronic pacemaker would be activated. While the patient would be protected from asystole (a total absence of any heartbeat), the loss of appropriate AV synchrony combined with the slow rate was often hemodynamically inefficient, i.e., the efficiency of the heart as a pump was compromised.
One approach to remedying this inefficiency utilizes a hysteresis circuit, in which the hysteresis escape rate of the pacemaker is slower than the automatic rate. When the hysteresis circuit was invoked, the patient's underlying cardiac rhythm is permitted to persist until the heart rate falls below a hysteresis escape rate. When this happens, there is one cycle of pacing at the hysteresis escape rate followed by pacing at a more rapid rate until a conducted R-wave is sensed. When the conducted R-wave is sensed, the hysteresis escape rate is restored to again inhibit the pacemaker and allow underlying cardiac rhythm to persist.
A number of heretofore unsolved problems exist with hysteresis. One problem is confusion on the part of the medical personnel caring for the patient as to why the patient's underlying rhythm occurs at a slower rate than the automatic rate to which the pacemaker is set. A second problem is that the slow atrial escape rate promotes the occurrence of premature ventricular contractions (PVC's), ectopic beats, or pathologic R-waves. In operation, the electronic circuits of the pacemaker sense a PVC as an R-wave, and therefore assume that natural conduction has returned, and that therefore the pacing at the more rapid rate is no longer needed. As a result, the escape interval of the pacemaker is reset to the slower hysteresis escape rate following each PVC, thereby effectively maintaining a slower cardiac rate.
In view of the above problems, (confusion on the part of the medical community, and the repeated resetting of the pacemaker to a slower rate by the occurrence of PVC'S) hysteresis was not well accepted by the medical community until such time as it was introduced as a programmable parameter capable of being enabled or disabled, and when enabled, capable of being adjusted so that the degree of hysteresis (i.e., the difference between the slow and fast atrial escape rates) could be changed.
Since the goal of hysteresis is to allow the patient's underlying rhythm with appropriate AV synchrony for as much time as possible, while providing pacing support at a hemodynamically efficient rate at only those times when the patient requires such support, hysteresis was not incorporated into the first dual-chamber pacing systems, which were designed to always provide hemodynamically efficient AV synchrony. Some physicians, however, recognized that some patients, whose heart rate precipitously and abruptly slowed, not only needed a more rapid cardiac rate at these times, but they also required AV synchrony. Problematically, if the base rate of the typical dual-chamber pacemaker is programmed to a rate required when cardiac pacing is needed by such patients, the electronic pacemaker frequently controls the patient's rhythm even when cardiac pacing is not needed. In an attempt to solve this problem, adaptations were introduced into some of the first generation dual-chamber electronic pacemakers to allow hysteresis in the DDI mode. This allowed the electronic pacemaker to remain inhibited in the presence of sensed cardiac signals, and to stimulate only when the electronic pacemaker was needed. Once activated, the electronic pacemaker will then pace in both atrium and ventricle while tracking at the atrial rate until such time as an R-wave was sensed, thereby inhibiting the generation of a V-pulse. Once inhibited, hysteresis would required expiration of the hysteresis escape interval before the electronic pacemaker again released output pulses.
Several problems persist in the application of hysteresis in the DDI mode. The first is that PVC's, a limitation first noted with single-chamber hysteresis systems, may be equally limiting in the dual-chamber pacing mode. The second is that when pacing is required, patients often need a relatively short AV interval for optimum hemodynamic function. However, setting a short AV interval could result in the pacemaker usurping control of the heart's normal conduction system, resulting in sustained periods of pacing when it is no longer required. On the other hand, setting a long AV interval, while resulting in appropriate pacing system inhibition when pacing therapy is not required, may allow AV conduction when pacing is required, causing repeated reinitiation of the longer hysteresis escape interval. Consequently, sustained pacing at the relatively slow hysteresis escape rate may result, which (while appropriate for a few cardiac cycles) may not be appropriate for sustained periods of pacing. An electronic pacemaker that overcomes these problems would be highly desirable.
An additional problem exists when hysteresis is utilized in an AAI(R) mode of operation, namely, AAI(R) pacemaker syndrome. AAI(R) pacemaker syndrome exists when the heart rate (i.e., atrial paced rate) increases or an A-A interval shortens (whether due to the programmed automatic rate or under rate responsive sensor drive), but the A-R interval does not shorten. As a result, an atrial output pulse (A-pulse), which causes an atrial contraction, is generated coincident with the preceding conducted ventricular contraction (R-wave). When this occurs, the atrium contracts against a closed A-V valve, and therefore, is unable to force blood into the ventricle (which is also contracting). As a result, poor hemodynamic efficiency is achieved.
From the above, it is evident that improvements in the use of hysteresis in dual-chamber pacemakers are needed and desirable.